Another compound invented during that era, diethylstilbestrol, turned out to be more powerful as an estrogen, so bisphenol A was shelved... until polymer chemists discovered that it could be polymerized to form polycarbonate plastic. Unfortunately, the ester bond that links BPA monomers to one another to form a polymer is not stable and hence the polymer decays with time, releasing BPA into materials with which it comes into contact, for example food or water.

Bisphenol A is now deeply imbedded in the products of modern consumer society, not just as the building block for polycarbonate plastic (from which it then leaches as the plastic ages) but also in the manufacture of epoxy resins and other plastics, including polysulfone, alkylphenolic, polyalylate, polyester-styrene, and certain polyester resins.

Its
uses don't end with the making of plastic. Bisphenol A has been
used as an inert ingredient in pesticides (although in the US this
has apparently been halted), as a fungicide, antioxidant, flame
retardant, rubber chemical, and polyvinyl chloride stabilizer.

These
uses create a myriad of exposures for people. Bisphenol A-based
polycarbonate is used as a plastic coating for children's teeth
to prevent cavities, as a coating in metal cans to prevent the metal
from contact with food contents, as the plastic in food containers,
refrigerator shelving, baby bottles, water bottles, returnable containers
for juice, milk and water, micro-wave ovenware and eating utensils.

BPA
contamination is also widespread in the environment. For example,
BPA can be measured in rivers and estuaries at concentrations that
range from under 5 to over 1900 nanograms/liter. Sediment loading
can also be significant, with levels ranging from under 5 to over
100 µg/kg (ppb) BPA is quite persistent as under normal conditions
in the environment it does not readily degrade (Rippen
1999).

What
this all means is that most of your life you are within arm's length
or closer to bisphenol A. No wonder the
debate over its toxicity is so intense.

Some
important recent studies of bisphenol A:

Experiments with rats demonstrate that low level exposure to bisphenol A during fetal growth causes breast cancer in adults. At all levels tested down to 2.5 parts per billion, BPA induced formation of aberrant cell growth patterns associated in rodents and people with breast cancer. Levels only 5 times higher than EPA's current safe level caused carcinoma in situ. Using these results to set safety standards would radically reduce use of BPA in plastics and resins. More...

In utero exposure to BPA causes long-term effects on mammary tissue development in rats, increasing risks to cancer, and also increases sensitivity to a chemical known to cause breast cancer. The study strengthens support for a link between increasing rates of breast cancer in recent decades and increasing exposure to estrogenic chemicals like BPA. It also indicates that human epidemiological studies that fail to incorporate developmental exposures can't be trusted to identify cancer-causing agents. More...

Perinatal exposure to extremely low levels of bisphenol A causes precancerous prostate lesions in rats. These lesions, called prostatic intraepithelial neoplasia, or PIN, are cancerous and are considered to be a precursor of metastatic prostate cancer in humans. One hundred percent of rats exposed perinatally and then, during adulthood, treated with estradiol and testosterone to create hormonal conditions analogous to thos of an ageing man, developed high-grade PIN. The effect appears to result from the failure in exposed animals of a gene to become hypermethylated as the rats aged. More...

Experiments with mice reveal that chronic adult exposure to bisphenol A causes insulin resistance. Insulin resistance in people leads to Type II diabetes and congestive heart failure, and is part of the modern epidemic of 'metabolic syndrome.' The exposure levels used were within the range that people experience regularly. More...

In a small prospective study, researchers in Japan report that bisphenol A levels are higher in women with a history of repeated spontaneous miscarriages. This research was based on proof that BPA causes meiotic aneuploidy in mice. Meiotic aneuploidy is the commonest cause of miscarriage in people. The researchers also followed the pregnancies of the women to completion, and found evidence of aneuploidy in several of the miscarried fetuses.More...

Bisphenol A and the birth control pharmaceutical ethinylestradiol cause adverse effects in prostate development in mice at levels to which millions of Americans are exposed each year. The results implicate these compounds in human prostate diseases, including prostate cancer. The research also shows the futility of predicting the developmental consequences of low-dose exposures based on high-dose experiments. More...

A flood of new information about bisphenol A revealing both widespread human exposure and effects at extremely low doses sparks a call for a new risk assessment of the ubiquitous compound. Bisphenol A, the basic building block of polycarbonate plastic, alters development of the reproductive tract, the immune system, increases prostate tumor proliferation, changes brain chemistry and structure and affects an array of behaviors, including hyperactivity. Of 11 studies of the compound's effects at low doses, none funded by industry reported impacts. In contrast, 94 out of 104 government-funded studies found effects. This summary includes audio files of an international teleconference about bisphenol A. More...

Bisphenol A at extremely low levels causes changes in brain structure and behavior in rats. The locus coeruleus is believed to be a key brain center for anxiety and fear. Normally this is larger in females than in males. Rats exposed to BPA at levels beneath the current 'safe' exposure level established by the US EPA show a reversal in sex dimorphism, with males' LC larger than females.' .Kubo, K, O Arai, M Omura, R Wantanabe, R Ogata, and S Aou. 2003. Low dose effects of bisphenol A on sexual differentiation of the brain and behavior in rats. Neuroscience Research 45: 345-356.

An
accident in the lab, followed by careful analysis and a series of
experiments, reveals that bisphenol A causes aneuploidy
in mice at low levels of exposure. Because aneuploidy in
humans causes spontaneous miscarriages and some 10-20% of all birth
defects, including Down Syndrome, this implicates bisphenol A in
a broad range of human developmental errors.Hunt,
PA, KE Koehler, M Susiarjo, CA Hodges, A Ilagan, RC Voigt, S Thomas,
BF Thomas and TJ Hassold. 2003. Bisphenol
A exposure causes meiotic aneuploidy in the female mouse.
Current Biology 13: 546-553.

Experiments
by researchers at the University of Missouri raise the possibility
of widespread contamination of laboratory experiments by
bisphenol A. Their results demonstrate that at room temperature
significant amounts of this estrogenic substance leach into water
from old polycarbonate animal cages. This
inadvertent contamination could interfere with experiments
designed to test the safety of estrogenic chemicals, and
lead to false negatives and conflicting results.Howdeshell, KA, PH Peterman, BM Judy, JA Taylor,
CE Orazio, RL Ruhlen, FS vom Saal, and WV Welshons 2003. Bisphenol
A is released from used polycarbonate animal cages into water at
room temperature. Environmental Health Perspectives
doi:10.1289/ehp.5993.

Using
new analytical methods, a team of German scientists measured bisphenol
A in the blood of pregnant women, in umbilical blood at birth and
in placental tissue. All samples examined contained BPA,
at levels within the range shown to alter development. Thus
widespread exposure to BPA at levels of concern is no longer a hypothetical
issue. It is occurring.Schönfelder,
G, W Wittfoht, H Hopp, CE Talsness, M Paul and I Chahoud. 2002.
Parent
Bisphenol A Accumulation in the Human Maternal-Fetal-Placental Unit.
Environmental Health Perspectives 110:A703-A707.

At
extremely low levels, BPA promotes fat cell (adipocyte) differentiation
and accumulation of lipids in a cell
culture line used as a model for adipocyte formation. These two
steps, differentiation and accumulation, are crucial in the development
of human obesity. Hence this result opens up a whole new chapter
in efforts to understand the origins of the world-wide obesity epidemic.
Masuno, H, T Kidani, K Sekiya, K Sakayama, T Shiosaka, H Yamamoto
and K Honda. 2002. Bisphenol
A in combination with insulin can accelerate the conversion of 3T3-L1
fibroblasts to adipocytes. Journal of Lipid Research
3:676-684.